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YAP在牵张力介导的人牙周膜细胞成骨分化中的作用

杨洋 韩光丽

临床口腔医学杂志2018,Vol.34Issue(2):67-70,4.
临床口腔医学杂志2018,Vol.34Issue(2):67-70,4.DOI:10.3969/j.issn.1003-1634.2018.02.002

YAP在牵张力介导的人牙周膜细胞成骨分化中的作用

Role of YAP in tension force-induced osteogenesis of human periondontal ligament cells

杨洋 1韩光丽1

作者信息

  • 1. 武汉大学口腔医学院口腔基础医学省部共建国家重点实验室培训基地和口腔生物医学教育部重点实验室 湖北 武汉 430079
  • 折叠

摘要

Abstract

Objective:To investigate the role of Yes-associated protein(YAP)in tension force-induced osteoblast differentiation in human periodontal ligament cells.Methods:HPDLCs were acquired by enzyme digestion method.Firstly,the cells were stretched and subjected to immunofluorescence assay to detect the changes of YAP location in hPDLCs,after being stretched for 1 d and 3 d,the qRT-PCR and alkaline phosphatase staining assay were performed respectively to detect the ex-pression of osteogenesis-related genes(ALP,DLX5,RUNX2)and ALP activity.Secondly,hPDLCs were transfected with YAP SiRNA or negative control SiRNA and stretched for 1 d and 3 d,osteogenesis-related genes and alkaline phosphatase staining assay were used to analyse the influence of YAP on tension force-induced osteogenic differentiation of hPDLCs.Results:Nu-clear localization of YAP was significantly facilitated by tension force,and compared with control,stretched hPDLCs showed remarkable increase in osteogenesis-related genes and ALP activity.After transfection with YAP SiRNA,the expression of os-teogenesis-related genes and ALP activity were significantly attenuated in stretched hPDLCs,compared with those transfected with negative control SiRNA.Conclusion:YAP knockdown leads to inhibition of tension force-induced osteogenesis in hP-DLCs,and it may serve as a new therapeutic target for orthodontic treatment.

关键词

人牙周膜细胞/成骨分化/Yes相关蛋白/牵张力

Key words

Human periodontal ligament cells/Osteogenic differentiation/Yes-associated protein/Tension force

分类

医药卫生

引用本文复制引用

杨洋,韩光丽..YAP在牵张力介导的人牙周膜细胞成骨分化中的作用[J].临床口腔医学杂志,2018,34(2):67-70,4.

基金项目

国家自然科学基金面上项目(81371169,81771111) (81371169,81771111)

临床口腔医学杂志

OACSTPCD

1003-1634

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